Doxorubicin–DNA complex

The "Doxorubicin–DNA complex" describes the physical and functional ensemble formed when doxorubicin, an anthracycline chemotherapy agent, **intercalates between base pairs of DNA**—preferentially at GC-rich regions—through planar ring stacking and hydrogen bonding, resulting in local distortion of the double helix[1][2][4][5][6][7]. This drug–DNA interaction can be either non-covalent (intercalation) or, under the influence of formaldehyde, covalent (adduct formation), especially at clinical concentrations[1]. This complex **disrupts DNA and chromatin architecture** and inhibits critical functions such as DNA replication and transcription, predominantly through the inhibition of topoisomerase II, an enzyme required to manage DNA topology during these cellular processes[2][3][4][6]. Additional mechanisms include the induction of DNA strand breaks, formation of DNA adducts, and generation of reactive oxygen species, all leading ultimately to apoptotic cell death[2][6]. "Doxorubicin–DNA complex" is not a conventional therapeutic target, but rather the intended cytotoxic product of doxorubicin’s action on its primary macromolecular substrate, DNA[1][2][6]. Thus, this entry is not suitable as a canonical or structured target name in drug discovery or pharmacology databases.

Other names

doxorubicin–DNA adductDOX–DNA complex

DNA intercalation, inhibition of DNA topoisomerase II, DNA adduct formation, induction of DNA strand breaks, generation of reactive oxygen species